nf-κb-in-1

NF-κB-IN-1 (1,6-Heptadiene-3,5-dione, 1,7-bis(3,4-dimethoxyphenyl)-4-[(4-hydroxy-3-methoxyphenyl)methylene]-, (1E,6E)-) is a potent NF-κB signaling pathway inhibitor. It is a 4-arylidene crucumin analogue. NF-κB-IN-1 directly inhibits IKK to block NF-κB activation. NF-κB-IN-1 effectively inhibits the viability of lung cancer cells and attenuates the clonogenic activity of A549 cells.

TLR4 NF-κB-IN-1 (Compound 7x) is an orally bioavailable inhibitor targeting the TLR4 NF-κB signaling pathway, with anti-inflammatory properties and the ability to cross the blood-brain barrier. It can alleviate LPS-induced acute neuroinflammation in mice and downregulate the protein expression of TLR4, P-NF-κB, and P-IκB-α.

Akt NF-κB JNK-IN-1 (Compound 2i) is an inhibitor of the Akt, NF-κB, and JNK signaling pathways, demonstrating inhibition of nitric oxide production (IC50: 3.15 μM) and exhibiting anti-inflammatory effects.

TLR4 NF-κB MAPK-IN-1 is a novel antineuroinflammatory agent inhibiting the TLR4 NF-κB MAPK pathways.

NF-κB PON1-IN-1 (Compound 16) is an inhibitor of the NF-κB PON1 pathway, exhibiting antioxidant activity (IC50: 45.76 μM) and hepatoprotective properties.

NF-κB MAPK-IN-1 is a potent dual inhibitor of the NF-κB and MAPK pathways with potential anti-inflammatory activity, inhibition of NO production, and inhibition of LPS-induced activation of iNOS, COX-2, ERΚ and P38. NF-κB MAPK-IN-1 is used for the prevention and treatment of rheumatoid arthritis (RA).

NF-κB-IN-10 (compound E1) is an NF-κB inhibitor that mitigates heart failure symptoms by modulating the Nrf2 NF-κB signaling pathway, alleviating oxidative stress and inflammation. It suppresses LPS-induced NO production and downregulates iNOS and COX-2 expression in RAW264.7 cells, showing potential for cardiovascular disease research [1].

Akt NF-κB MAPK-IN-1 (compound 2m) is a potent, orally active inhibitor of NO with an IC50 of 7.70 μM and low toxicity, exhibiting anti-inflammatory effects by blocking the Akt NF-κB and MAPK signaling pathways [1].

NF-κB-IN-12 (compound 3h) is a potent NF-κB inhibitor with an IC50 of 1.02 μM, suitable for research in acute lung injury [1].

NF-κB-IN-11 (Compound 3i) is an inhibitor of NF-κB, effectively blocking TNF-α-induced NF-κB pathway activation and nuclear translocation of NF-κB, alongside reducing expression levels of phospho-IKK, IκBα, and NF-κB p65. Demonstrating anti-inflammatory properties, it mitigates dextran sulfate sodium-induced colitis in mice and exhibits a maximum tolerated dose (MTD) exceeding 1852 mg kg in acute toxicity assays when administered orally (p.o.) [1].

NF-κB-IN-13 (compound 12) significantly inhibits LPS-induced NF-κB activation and NO synthesis in RAW264.7 macrophages, demonstrating anti-inflammatory properties [1].

NF-κB-IN-18 (Compound 5k) is an orally active NF-κB inhibitor that suppresses the phosphorylation of p65 and demonstrates significant anti-inflammatory activity in mice with xylene-induced ear edema.

NF-κB-IN-19 (Compound 8) is an NF-κB inhibitor. It effectively induces DNA damage in tumor cells through the NF-κB signaling pathway and promotes the production of reactive oxygen species (ROS), as well as induces autophagy and apoptosis. Additionally, NF-κB-IN-19 inhibits levels of VEGF and HIF-1α, exerting antiproliferative effects in tumor cells through the PI3K AKT and STAT-3 pathways. It is also effective in overcoming cisplatin resistance and exhibits antitumor activity.

NF-κB-IN-17 (Zinc5) is an inhibitor of NF-κB. It inhibits the binding activity of NF-κB DNA in C2C12 cells induced by TNF-α.

5-Aminosalicylic Acid (5-ASA) is an anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE.

NF-κΒ activator 1 can activate the nf-kappa Β gene activator, EC50 of 0.9 microns. NF-κΒ is widely used in eukaryotic cells as a gene regulating cell proliferation and cell survival. NF-κΒ activator 1 induces superoxide dismutase (SOD) 2 1 mRNA expression.

LTβR-IN-1 is a potent and selective lymphin β receptor (LTβR) inhibitor with a selective inhibitory effect on the nuclear translocation of p52 of TNF12A, without affecting the nuclear translocation of p65 mediated by the TNF-α receptor. It inhibits p52 nuclear translocation stimulated by TWEAK or Anti-LTβR with an IC50 of 10 μM and regulates the NF-kB signaling pathway in a ligand-independent manner.

Inflachromene (ICM) is an inhibitor of HMGB1 and HMGB expression with anti-inflammatory activity.Inflachromene reduces seizure severity in a mouse model of epilepsy by inhibiting HMGB1 translocation, inhibits endothelial proliferation through the HMGB1 2-regulated TLR4-NF-κB pathway, and inhibits autophagy by regulating Beclin 1 activity. Inflachromene can be used to study epilepsy.

AP-1 NF-κB activation inhibitor 1 is a potent inhibitor of AP-1 and NF-κB mediated transcriptional activation (IC50 = 1 μM), without blocking basal transcription driven by the β-actin promoter. It has a similar inhibitory effect on the production of IL-2 and IL-8 levels in stimulated cells [1].

Lidocaine (Alphacaine) is an amide local anesthetic with anti-inflammatory properties in vitro and in vivo. It has this functions perhaps due to an attenuation of intracellular adhesion molecule-1 (ICAM-1), pro-inflammatory cytokines, and reduction of neutrophils influx.

α-Lipoic Acid (Alphalipoic acid) inhibits NF-κB-dependent HIV-1 LTR activation. α-Lipoic Acid induces endoplasmic reticulum (ER) stress-mediated apoptosis in hepatoma cells.α-Lipoic Acid is an antioxidant, which is an essential cofactor of mitochondrial enzyme complexes.

1. Linalool (Linalol), a natural compound of the essential oils, has been shown to have antinociceptive, antimicrobial, and anti-inflammatory properties. 2. Linalool was protected against LPS GalN-induced liver injury through induction of antioxidant defense via Nrf2 activating and reduction inflammatory response via NF-κB inhibition. 3. Linalool biosynthesis and accumulation might be involved in plant defense against bacterial and fungal pathogens and be associated with field resistance to citrus canker. 4. Linalool significantly increased the expression of antioxidant enzymes regulated by Nrf-2 and diminished lung tissue levels of several pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin (IL)-6.

Fumaric acid (2-Butenedioic acid) attenuates the eotaxin-1 expression in TNF-α-stimulated fibroblasts by suppressing p38 MAPK-dependent NF-κB signaling. Fumaric acid has recently been identified as an oncometabolite or an endogenous, cancer-causing metabolite. High levels of this organic acid can be found in tumors or biofluids surrounding tumors. Its oncogenic action appears due to its ability to inhibit prolyl hydroxylase-containing enzymes.

NSC-37445 has anti-tumor activity, such as inhibits growth of bladder tumor cells in a nude mice model , prevents the recurrence and progression of non-muscle-invasive urothelial cell carcinoma. NSC-37445 can significantly reduce the expression of CDK1-inhibitory kinases, Myt1 and Wee1, and cause cyclin B1 protein accumulation leading to CDK1 activation in T24 cells. 3. Flavokawain A (Flavokavain A) may exert anti-inflammatory responses by suppressing LPS-induced expression of pro-inflammatory mediators via blockage of NF-κB-AP-1-JNK p38 MAPK signaling pathways in the murine macrophages.